Modulation of Respiratory Neural Drive by Physiological Loads in COVID-19 Patients with Dyspnea

COVID-19 patients often experience dyspnea due to several factors. The underlying unique pathophysiology of dyspnea in COVID-19 is not yet fully understood, but it is believed to be related to a combination of respiratory, cardiovascular, and neuromuscular factors. Hypoxemia is considered one of the key symptoms of COVID-19. This affects the respiratory drive, which determines the rate, depth, and pattern of breathing. The relationship between increased ventilatory neural drive and abnormal gas exchange, particularly in the context of ventilation/perfusion (V/Q) mismatches and chemosensitivity, has gained significant attention following the COVID-19 pandemic. The ACE2 receptors allow viral entry into the lungs, leading to the loss of surfactant, hypoxic vasoconstriction, and intrapulmonary shunting that may result in a V/Q mismatch. Additionally, acidosis, hypercapnia, elevated 2,3-diphosphogly-cerate levels and fever may shift the oxygen diffusion curve rightward, lowering arterial oxygen saturation levels and triggering ventilatory responses. This paper examines how physio pathological factors such as altered gas diffusion, chemosensory feedback, V/Q ratios, altered compliance, arterial blood gases, and respiratory muscle dysfunction in these patients affect ventilatory drive. A review of the published literature was also conducted to determine the mechanism of dyspnea. To ensure appropriate gas exchange, individuals need to augment their minute ventilation (VE) when physiological dead space is elevated. This serves as a compensatory mechanism to counteract the effects of compromised gas exchange and keep adequate oxygenation throughout the body. The respiratory centers may experience dysregulation due to the impact of the virus on the respiratory system, which could affect the rhythm-generating and pattern-generating signals that are vital for regulating the respiratory rate and depth of breathing effort. The cerebral cortex, in conjunction with the brain stem centers, plays a crucial role in regulating ventilation during prolonged hypoxemia. This interaction between these two components may help elucidate the conscious respiratory sensation (or dyspnea) experienced by patients. It is hypothesized that neuroventilatory decoupling acts as a mechanism to prevent sensory signals from translating into mechanical or ventilatory responses. This decoupling phenomenon is believed to have a notable impact on the intensity of breathlessness. By understanding the relationship between increased ventilatory neural drive and abnormal gas exchange, particularly in the context of ventilation/perfusion (V/Q) mismatches and altered chemosensitivity, healthcare professionals can develop strategies to optimize respiratory support for COVID-19 patients.